Human diabetes mellitus is not a single disease, but rather a group of disorders having in common, hyperglycemia. Hyperglycemia may accompany a spectrum of insulin states, ranging from absolute deficiency of insulin, to extreme insensitivity to the actions of insulin. No classification of the human diabetic syndrome is entirely satisfactory but at least two large categories have been accepted by most diabetologists (Insulin-dependent and non-insulin dependent). As complicated and difficult to categorize the human diabetic syndromes an enormous panoply of distinct animal diabetic syndromes exist. Although it may be tempting to squeeze the animal diabetic syndromes into the human categories, one must be exceptionally cautious in performing such a maneuver. Animal models of diabetes can be simply classified as either hypoinsulinemia or hyperinsulinemia. Marked decrease of insulin levels have been found in various experimental animal models. Two models which have recently been studied in our laboratory include the BB rat and the multiple-dose SZ model. BB Rat. In approximately 1/3 of an outbred strain of Wistar derived rats develop insulin dependent diabetes. At approximately 60-120 days of age an acute absolute insulin deficiency occurs with various biochemical parameters as observed in the human counterpart. Hyperglucagonemia, elevated free-fatty acids, ketosis, occurs and unless treated with exogenous insulin the animals succumb. During this acute phase histopathologic studies of islets reveal a mononuclear infiltration surrounding the islets (insulitis). Following the acute episode the disappearances of these inflammatory cells occurs with the disappearances of beta cells while non-beta cells remain within the islets. The syndrome occurs at an equal frequency in animals gnotobiotically derived and is, therefore, not infectious in origin. Recent studies have suggested that immunosuppression with anti-lymphocyte serum can ameliorate acutely diabetic animals and more importantly, present the occurrence in susceptible animals. Multiple Dose SZ-Model. Another approach in including diabetes in experimental animals has been by selective destruction of the beta cells. If SZ is given in small multiple doses (no one alone would be diabetogenic) it will produce in mice as delayed but progressive hyperglycemia. Paripassau with the hyperglycemia is the presence of insulitis and the induction o (Text Truncated - Exceeds Capacity)